Ser18 and Ser23 Phosphorylation Plays Synergistic Roles in Activating p53-Dependent Neuronal Apoptosis
نویسندگان
چکیده
منابع مشابه
Ser18 and 23 phosphorylation is required for p53-dependent apoptosis and tumor suppression.
Mouse p53 is phosphorylated at Ser18 and Ser23 after DNA damage. To determine whether these two phosphorylation events have synergistic functions in activating p53 responses, we simultaneously introduced Ser18/23 to Ala mutations into the endogenous p53 locus in mice. While partial defects in apoptosis are observed in p53S18A and p53S23A thymocytes exposed to IR, p53-dependent apoptosis is esse...
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Phosphorylation of mouse p53 at Ser18 occurs after DNA damage. To determine the physiological roles of this phosphorylation event in p53-dependent DNA damage responses, a Ser18 to Ala missense mutation was introduced into the germline of mice. Thymocytes and fibroblasts from the knock-in mice show reduced transactivation of many p53 target genes following DNA damage. p53 protein stabilization a...
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P ho sp ho ry la ti o n N-Terminal: S6, S9, S15, T18, S20 ATM, DNAPK, • CK1 ERKs, ATR, p38 • kinase, mTOR, Chk1/Chk2, JNK, MAPKAP2, Hipk4 Activated by DNA damage, UV light, ionizing radiation, replicative senes• cence, or phosphatidylcholines. N-terminal phosphorylation causes p53 stabilization by inhibiting the p53• MDM2 interaction. Knockin mice carrying separate analogs to human Ser18/ • Ser...
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Previous studies have shown that zinc deficiency leads to apoptosis of neuronal precursor cells in vivo and in vitro. In addition to the role of p53 as a nuclear transcription factor in zinc deficient cultured human neuronal precursors (NT-2), we have now identified the translocation of phosphorylated p53 to the mitochondria and p53-dependent increases in the pro-apoptotic mitochondrial protein...
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ژورنال
عنوان ژورنال: Cell Cycle
سال: 2007
ISSN: 1538-4101,1551-4005
DOI: 10.4161/cc.6.12.4391